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  1. Article ; Online: Hepatitis E Virus Genotype 3 Genomes from RNA-Positive but Serologically Negative Plasma Donors Have CUG as the Start Codon for ORF3.

    Norder, Heléne / Galli, Cristina / Magnil, Ellen / Sikora, Per / Ekvärn, Elisabet / Nyström, Kristina / Magnius, Lars O

    Intervirology

    2018  Volume 61, Issue 2, Page(s) 96–103

    Abstract: Hepatitis E virus (HEV) is a pathogen that causes hepatitis worldwide. Molecular studies have identified HEV RNA in blood products although its significance is not understood. This study was undertaken to characterize HEV genomes in asymptomatic plasma ... ...

    Abstract Hepatitis E virus (HEV) is a pathogen that causes hepatitis worldwide. Molecular studies have identified HEV RNA in blood products although its significance is not understood. This study was undertaken to characterize HEV genomes in asymptomatic plasma donors from Sweden and Germany lacking anti-HEV. Complete open reading frames (ORFs) were obtained from HEV strains in 5 out of 18 plasma donors who tested positive for HEV RNA. All strains had CUG as the start codon of ORF3, while 147 GenBank strains all had AUG as the start codon (p < 0.0001). This substitution was found in both interrelated and unrelated strains belonging to different phylogenetic clades. The HEV strains from the seronegative plasma donors had no other substitution in common, which may be why the CUG substitution seems to explain the seronegativity.
    MeSH term(s) Amino Acid Sequence ; Blood Donors ; Codon, Initiator ; Genome, Viral ; Genotype ; Hepatitis E/virology ; Hepatitis E virus/classification ; Hepatitis E virus/genetics ; Hepatitis E virus/immunology ; Humans ; Immunoglobulin G/immunology ; Immunoglobulin M/immunology ; Open Reading Frames ; Phylogeny ; RNA, Viral ; Viral Proteins/chemistry ; Viral Proteins/genetics
    Chemical Substances Codon, Initiator ; Immunoglobulin G ; Immunoglobulin M ; ORF3 protein, Hepatitis E virus ; RNA, Viral ; Viral Proteins
    Language English
    Publishing date 2018-10-02
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 184545-7
    ISSN 1423-0100 ; 0300-5526
    ISSN (online) 1423-0100
    ISSN 0300-5526
    DOI 10.1159/000491926
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1040: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  2. Article ; Online: Paladin is a phosphoinositide phosphatase regulating endosomal VEGFR2 signalling and angiogenesis.

    Nitzsche, Anja / Pietilä, Riikka / Love, Dominic T / Testini, Chiara / Ninchoji, Takeshi / Smith, Ross O / Ekvärn, Elisabet / Larsson, Jimmy / Roche, Francis P / Egaña, Isabel / Jauhiainen, Suvi / Berger, Philipp / Claesson-Welsh, Lena / Hellström, Mats

    EMBO reports

    2020  Volume 22, Issue 2, Page(s) e50218

    Abstract: Cell signalling governs cellular behaviour and is therefore subject to tight spatiotemporal regulation. Signalling output is modulated by specialized cell membranes and vesicles which contain unique combinations of lipids and proteins. The ... ...

    Abstract Cell signalling governs cellular behaviour and is therefore subject to tight spatiotemporal regulation. Signalling output is modulated by specialized cell membranes and vesicles which contain unique combinations of lipids and proteins. The phosphatidylinositol 4,5-bisphosphate (PI(4,5)P
    MeSH term(s) Animals ; Endothelial Cells/metabolism ; Mice ; Neovascularization, Physiologic ; Phosphatidylinositol 4,5-Diphosphate ; Phosphoinositide Phosphatases ; Phosphoprotein Phosphatases ; Signal Transduction ; Vascular Endothelial Growth Factor Receptor-2/genetics ; Vascular Endothelial Growth Factor Receptor-2/metabolism
    Chemical Substances Phosphatidylinositol 4,5-Diphosphate ; Vascular Endothelial Growth Factor Receptor-2 (EC 2.7.10.1) ; Pald1 protein, mouse (EC 3.1.3.16) ; Phosphoprotein Phosphatases (EC 3.1.3.16) ; Phosphoinositide Phosphatases (EC 3.1.3.36)
    Language English
    Publishing date 2020-12-28
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2020896-0
    ISSN 1469-3178 ; 1469-221X
    ISSN (online) 1469-3178
    ISSN 1469-221X
    DOI 10.15252/embr.202050218
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5433: Show issues Location:
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  3. Article: Hepatitis E Virus Genotype 3 Genomes from RNA-Positive but Serologically Negative Plasma Donors Have CUG as the Start Codon for ORF3

    Norder, Heléne / Galli, Cristina / Magnil, Ellen / Sikora, Per / Ekvärn, Elisabet / Nyström, Kristina / Magnius, Lars O.

    Intervirology

    2018  Volume 61, Issue 2, Page(s) 96–103

    Abstract: Hepatitis E virus (HEV) is a pathogen that causes hepatitis worldwide. Molecular studies have identified HEV RNA in blood products although its significance is not understood. This study was undertaken to characterize HEV genomes in asymptomatic plasma ... ...

    Institution Department of Infectious Diseases, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
    Department of Biomedical Sciences for Health, University of Milan, Milan, Italy
    Department of Pathology and Genetics, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
    Clinical Genomics Gothenburg, SciLife Labs, Gothenburg, Sweden
    Octapharma AB, Stockholm, Sweden
    Ulf Lundahls Foundation, Stockholm, Sweden
    Abstract Hepatitis E virus (HEV) is a pathogen that causes hepatitis worldwide. Molecular studies have identified HEV RNA in blood products although its significance is not understood. This study was undertaken to characterize HEV genomes in asymptomatic plasma donors from Sweden and Germany lacking anti-HEV. Complete open reading frames (ORFs) were obtained from HEV strains in 5 out of 18 plasma donors who tested positive for HEV RNA. All strains had CUG as the start codon of ORF3, while 147 GenBank strains all had AUG as the start codon (p < 0.0001). This substitution was found in both interrelated and unrelated strains belonging to different phylogenetic clades. The HEV strains from the seronegative plasma donors had no other substitution in common, which may be why the CUG substitution seems to explain the seronegativity.
    Keywords HEV3 ; Blood donors ; Mutation ; Nucleotide sequence
    Language English
    Publishing date 2018-10-02
    Publisher S. Karger AG
    Publishing place Basel, Switzerland
    Document type Article
    Note Short Communication ; This article is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND).
    ZDB-ID 184545-7
    ISSN 1423-0100 ; 0300-5526
    ISSN (online) 1423-0100
    ISSN 0300-5526
    DOI 10.1159/000491926
    Database Karger publisher's database

    Full text online

    More links

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1040: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Gpr116 Receptor Regulates Distinctive Functions in Pneumocytes and Vascular Endothelium.

    Niaudet, Colin / Hofmann, Jennifer J / Mäe, Maarja A / Jung, Bongnam / Gaengel, Konstantin / Vanlandewijck, Michael / Ekvärn, Elisabet / Salvado, M Dolores / Mehlem, Annika / Al Sayegh, Sahar / He, Liqun / Lebouvier, Thibaud / Castro-Freire, Marco / Katayama, Kan / Hultenby, Kjell / Moessinger, Christine / Tannenberg, Philip / Cunha, Sara / Pietras, Kristian /
    Laviña, Bàrbara / Hong, JongWook / Berg, Tove / Betsholtz, Christer

    PloS one

    2015  Volume 10, Issue 9, Page(s) e0137949

    Abstract: Despite its known expression in both the vascular endothelium and the lung epithelium, until recently the physiological role of the adhesion receptor Gpr116/ADGRF5 has remained elusive. We generated a new mouse model of constitutive Gpr116 inactivation, ... ...

    Abstract Despite its known expression in both the vascular endothelium and the lung epithelium, until recently the physiological role of the adhesion receptor Gpr116/ADGRF5 has remained elusive. We generated a new mouse model of constitutive Gpr116 inactivation, with a large genetic deletion encompassing exon 4 to exon 21 of the Gpr116 gene. This model allowed us to confirm recent results defining Gpr116 as necessary regulator of surfactant homeostasis. The loss of Gpr116 provokes an early accumulation of surfactant in the lungs, followed by a massive infiltration of macrophages, and eventually progresses into an emphysema-like pathology. Further analysis of this knockout model revealed cerebral vascular leakage, beginning at around 1.5 months of age. Additionally, endothelial-specific deletion of Gpr116 resulted in a significant increase of the brain vascular leakage. Mice devoid of Gpr116 developed an anatomically normal and largely functional vascular network, surprisingly exhibited an attenuated pathological retinal vascular response in a model of oxygen-induced retinopathy. These data suggest that Gpr116 modulates endothelial properties, a previously unappreciated function despite the pan-vascular expression of this receptor. Our results support the key pulmonary function of Gpr116 and describe a new role in the central nervous system vasculature.
    MeSH term(s) Alveolar Epithelial Cells/metabolism ; Animals ; Blood-Brain Barrier/metabolism ; Blotting, Western ; Bronchoalveolar Lavage Fluid/chemistry ; Capillary Permeability/genetics ; Endothelium, Vascular/metabolism ; Female ; Gene Expression ; Homeostasis/genetics ; Lung/metabolism ; Lung/pathology ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Microscopy, Confocal ; Models, Biological ; Myocardium/metabolism ; Myocardium/pathology ; Pulmonary Surfactants/metabolism ; Receptors, G-Protein-Coupled/genetics ; Receptors, G-Protein-Coupled/metabolism ; Retinal Neovascularization/genetics ; Retinal Neovascularization/metabolism ; Spleen/metabolism ; Spleen/pathology
    Chemical Substances Gpr116 protein, mouse ; Pulmonary Surfactants ; Receptors, G-Protein-Coupled
    Language English
    Publishing date 2015
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0137949
    Database MEDical Literature Analysis and Retrieval System OnLINE

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